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PubMed1979

Dopamine--acetylcholine "balance" in nucleus accumbens and corpus striatum and its effect on hypothalamic self-stimulation.

Three experiments investigated the suppression of hypothalamic self-stimulation in rats by neuroleptics and its restoration by centrally acting anticholinergic agents. Scopolamine (0.1--1.0 mg/kg i.p.) and benztropine (1.0--10.0 mg/kg i.p.) each enhanced self-stimulation when administered alone, and partially restored performance suppressed by spiroperidol (0.05--0.15 mg/kg i.p.). Benztropine strongly inhibits transmitter reuptake at DA synapses but scopolamine does not, thus inhibition of DA reuptake cannot fully account for the stimulant or antineuroleptic action of anticholinergic drugs. Neuroleptic and anticholinergic effects on self-stimulation rate were mutually subtractive, and statistical evidence of interaction was not obtained. Scopolamine was shown also to restore performance extinguished by discontinuation of the stimulating current. Smaller doses of scopolamine (50 nmol; 19 microgram) injected directly into the nucleus accumbens septi partially restored responding suppressed by spiroperidol, though similar doses of scopolamine injected bilaterally into the caudate-putamen were ineffective. These findings suggest that hypothalamic self-stimulation may be influenced by ACh-and DA-containing systems which exert independent effects on a third system controlling performance. These effects appear to reflect the level of arousal or motivation rather than the reinforcement process itself.

Acetylcholine↗
PubMed1980

A genetically mediated relationship between the readiness to self stimulate lateral hypothalamus and the intensity of the septal and ventromedial hypothalamic rage syndromes.

Rats from two genetically high self stimulating lines (LC1-Hi, LC2-Hi) and from two genetically low self stimulating lines (LC1-Lo, LC2-Lo) were subjected to septal lesions at various ages. The genetically high self-stimulators exhibited the typical marked increase in emotionality following septal lesions, while the genetically low self stimulators showed an attentuated emotional response following septal lesions. In a subsequent experiment, animals from the same lines were subjected to VMH lesions. Once again, animals from the genetic high self stimulating lines showed a marked increase in emotionality following the lesions while the animals from the genetic low self-stimulating lines showed an attenuated emotional response. Hyperphagia was observed in all lines with no relation to the self stimulation genetic background. It is suggested that the septal and VMH systems modulating affective behavior are functionally related to the system modulating self stimulation, while these mechanisms seem to be basically independent of the VMH systems involved in maintenance of body weight.

Anger↗
PubMed1975

Differential effects of amphetamine and food deprivation of self-stimulation of the lateral hypothalamus and medial frontal cortex.

Intracranial self-stimulation of the lateral hypothalamus of the rat was markedly increased by d-amphetamine administration and by food deprivation. In contrast, similar self-stimulation response rates obtained in the same animals from the medial frontal cortex were unaffected by food deprivation and only slightly increased by d-amphetamine administration. Furthermore, a large difference between d- vs. l-amphetamine on response rate was obtained for lateral hypothalamic but not for medial frontal cortex self-stimulation. The results of this study were consistent with a noradrenergic self-stimulation system for the lateral hypothalamus. Medial frontal cortex self-stimulation, however, appears to be mediated by a neuroanatomical and neurochemical system different from that of the lateral hypothalamus.

Amphetamine↗
PubMed1994

The relationship between self-stimulation and sniffing in rats: does a common brain system mediate these behaviors?

The relationship between brain self-stimulation and brain-stimulation induced sniffing behavior was examined at three brain sites (frontal cortex, hypothalamus and lower brain stem). In the first experiment, sniffing was elicited in the prefrontal cortex and pontine reticular formation (PRF) of anesthetized rats. These sites corresponded to reported self-stimulation sites. In non-anesthetized animals (Expt. 2), all self-stimulation sites in the medial prefrontal cortex (MPC) and lateral hypothalamic-medial forebrain bundle (LH-MFB) also supported sniffing. In the PRF, this was also the case except for one subject which exhibited self-stimulation and jaw movements without sniffing. After unilateral lesions either in the MPC or PRF, stimulation-induced sniffing from the ipsilateral LH-MFB was not influenced. While MPC lesions did not affect self-stimulation either, medial PRF lesions disrupted ipsilateral self-stimulation. In summary, stimulation-induced sniffing and self-stimulation behavior appear to share strikingly similar anatomical loci, but the PRF appears to be differentially involved in these behaviors. The results were discussed from an appetitive motivational hypothesis of self-stimulation.

Animals↗
PubMed1973

Directionality of rewarding impulses within the medial forebrain bundle self-stimulation system of the rat.

Self-stimulation performance of rats was tested with conditioning pulses to the anterior preoptic area of the medial forebrain bundle followed at various intervals by test pulses to the contralateral posterior hypothalamic area of this bundle. Alternatively, conditioning pulses were delivered through the posterior electrode and test pulses were sent through the anterior electrode. The animals' performance in these two test sequences was indicative of (i) synaptic facilitation and (ii) a posterior convergence site of "self-stimulation impulses" in the medial forebrain bundle.

Animals↗
PubMed1996

Neurochemical mediators of anxiety have inconsistent effects on hypothalamic self-stimulation in rats.

We studied effects of anxiogenic and anxiolytic compounds on the electric self-stimulation of the medial fore-brain bundle in male rats to find out if there is a link between reward and anxiety-related behaviours. The cholecystokinin agonist, caerulein (25-100 micrograms/kg) and the 5-HT agonist 1-(3-chlorophenyl)piperazine (0.2-1 mg/kg) dose-dependently inhibited the electric self-stimulation. The 5-HT2A antagonist, ketanserin, at 2.5 mg/kg, increased the self-stimulation at high currents but not at threshold current. The 5-HT3 antagonist ondansetron (10 and 100 micrograms/kg). The alpha 1-adrenergic antagonist, prazosin (0.125 and 0.5 mg/kg), the beta-adrenergic antagonist, propranolol (5 and 10 mg/kg) and the alpha 2-adreno-receptor antagonist, atipamezole (4 mg/kg), did not affect the self-stimulation. Nor did the benzodiazepine agonist, diazepam (5-15 mg/kg), a benzodiazepine receptor antagonist flumazenil (at 10 and 25 mg/kg) or the inverse agonist of benzodiazepine receptors, N-methyl-beta-carboline-3-carboxamide (10 and 20 mg/kg), cause any substantial changes of the self-stimulation. We conclude that only two anxiolytic drugs (caerulein and 1-(3-chlorophenyl)piperazine) suppress the electric self-stimulation. These findings indicate that anxiogenicity as such is not able to weaken the hypothalamic electric self-stimulation. Anxiety and reward are apparently mediated through separate neural pathways.

Amphetamine↗
PubMed1991

Contrasting effects of stress on medial and sulcal prefrontal cortex self-stimulation.

Male Wistar rats were subjected to either 25 controllable or uncontrollable footshocks and then tested for changes in fixed-interval 5-second (FI-5) self-stimulation of the medial prefrontal cortex (MPC), sulcal prefrontal cortex (SPC) or nucleus accumbens (NAS). Controllable footshock caused a moderate facilitation of MPC self-stimulation (30% above baseline rates) but inhibited SPC self-stimulation (32% below baseline rates). Uncontrollable footshock had no effect on MPC self-stimulation but inhibited SPC self-stimulation (52% below baseline rates). An inhibition of SPC self-stimulation was also evident 24 hours following controllable or uncontrollable footshock. NAS self-stimulation was unaffected by footshock. Changes in locomotor activity were not consistently related to changes in self-stimulation following footshock. These results are discussed in terms of the different effects of mild stress on the release of reward-relevant neurotransmitters in the MPC, SPC and NAS. The possible role of stress-induced hypoalgesia in determining the stress-induced facilitation of MPC self-stimulation is also discussed.

Animals↗
PubMedDate not supplied

Comparison of the effects of dopamine agonists on self-stimulation of the hypothalamus with lesioning of mesolimbic brain structures in rats reared in conditions of social isolation.

Initial and phenamine-stimulated frequencies of self-stimulation of the lateral hypothalamus were not significantly different in rats reared in communities and in conditions of social isolation. Unilateral lesioning of the ventral tegmental area and the medial prefrontal cortex in early ontogenesis increased phenamine sensitivity only in isolated rats. The dopamine receptor agonist apomorphine, at a dose of 0.05 mg/kg, which affects presynaptic receptors, inhibited the self-stimulation response in intact group-reared animals and in rats reared in isolation, by 21-23%. Stimulation of the ventral tegmental area did not change, while stimulation of the medial prefrontal cortex doubled the sensitivity of rats to apomorphine in animals reared in isolation (at doses of 0.05 and 0.5 mg/kg). Conditions of partial sensory and complete species isolation resulted in the development of a state of presynaptic receptor hypersensitivity of dopamine receptors in mesocorticolimbic brain systems in rats.

Amphetamine↗
PubMed1975

Autonomic effects of hypothalamic self-stimulation in the cat.

Respiration, heart rate and arterial blood pressure were recorded continuously during self-stimulation with systematically varied stimulus parameters. Conspicuous autonomic effects were induced by self-stimulation. Acceleration in the respiration and heart rate, and rise in the arterial blood pressure were generally obtained as direct effects of the stimulus train, which were followed by remarkable rebound-like aftereffects. A close relationship was found between the lever-pressing behaviour and the peripheral autonomic effects of self-stimulation. The frequency of self-stimulation increased in parellel with the amplitude of the autonomic responses to a certain level, and the animal stopped self-stimulation whenever the amplitude of the autonomic effects exceeded this level. The results are consistent with the idea that the periopheral autonomic changes can modulate self-stimulation.

Animals↗
PubMed1992

Effects of amphetamine and nomifensine on intracranial self-stimulation discrimination behavior in rats.

Rats implanted with electrodes in the medial forebrain bundle-lateral hypothalamus were trained in a discrete trial procedure to make a differential response (right or left lever press) in the presence or absence of brain stimulation [intracranial self-stimulation (ICSS)]. When animals reached a high level of accuracy (95% correct) in the discrimination task, testing was begun. In the first experiment, we compared the effects of saline and 0.3 mg/kg d-amphetamine when the intertrial interval (ITI) was 1, 5, 10, and 15 s. In the second experiment, animals were tested either with saline, 0.3 mg/kg d-amphetamine, or 1, 3, or 10 mg/kg nomifensine and the ITI was held constant at 5 s. Increasing the ITI from 1-15 s did not produce a drug-induced change in the discriminative stimulus properties of ICSS, although it did produce changes in total numbers of lever presses and numbers of intertrial lever presses. In the second experiment, neither d-amphetamine nor nomifensine altered the discriminative stimulus properties of ICSS, but a dose-response increase occurred in the time to complete the test session and in total number of lever presses and in presses on the initiating lever. Under conditions known to increase extracellular dopamine (DA) levels in brain, both amphetamine and nomifensine produced large increases in locomotor activity, but neither drug produced changes in the detection threshold for ICSS. Results indicated that the internal cues produced by ICSS are different from those produced by these psychomotor stimulant drugs.

Amphetamine↗
PubMed1976

Catecholamines and self-stimulation: evidence suggesting a reinforcing role for noradrenaline and a motivating role for dopamine.

Investigation of the role of noradrenaline (NA) and dopamine (DA) in self-stimulation showed that d-amphetamine (which releases more DA than does l-amphetamine, but not more NA) was much more effective than l-amphetamine in enhancing self-stimulation of NA sites in the locus coeruleus and near-lateral hypothalamus. In DA sites in the substantia nigra and far-lateral hypothalamus the effects of the 2 isomers were confirmed to be more nearly equal. Thymoxamine HCl (10 mg/kg IP), a specific alpha-adrenergic receptor blocker, depressed self-stimulation at all sites, but significantly more severely at DA sites. Thus the drugs most effective in influencing self-stimulation at a particular site were those acting predominantly on the unstimulated system. These findings were interpreted in terms of a hypothesis that DA and NA play complementary roles in self-stimulation and that both are essential; or, more specifically, that DA pathways, implicated in other motivational activites, contribute to a state of drive or arousal necessary for self-stimulation; while response-contingent noradrenergic activity (elicited by the electrodes directly via a transsynaptic route) mediates reinforcement. Further predictions from this hypothesis were tested as follows: (1) Direct pharmacological stimulants of adrenergic alpha-receptors should disrupt self-stimulation by acting randomly on the reinforcement system and disrupting response-reward contingencies; this was confirmed by the finding that the alpha-receptor stimulant clonidine HCl (0.05 mg/kg) depressed self-stimulation at all sites tested. (2) Drect stimulants of DA receptors should enhance self-stimulation of NA sites by augmenting dopaminergic motivational activity; but in rats with DA electrodes, noncontingent stimulation of DA receptors would also impose similar noncontingent activity on the transsynaptic noradrenergic reinforcement pathways and thus depress self-stimulation; this was confirmed by the finding that apomorphine (0.3-1.0 mg/kg) was strongly stimulant for NA electrodes but strongly depressant for DA electrodes, and that the degree and direction of these effects was highly correlated with the differential effects of d- l-amphetamine (rho = .65, p less than 0.01). Neither effect of apomorphine depended on the occurrence of motor stereotypy. These results can be interpreted in terms of 2-component models for self-stimulation, with the predominant transmitter of the drive component being identified as DA and that g the reinforcing component as NA.

Amphetamine↗
PubMed1977

Differential effects of morphine and D-amphetamine on self-stimulation from closely adjacent regions in rat midbrain.

The effects of morphine were investigated on self-stimulation from numerous electrode placements in the area of the substantia nigra or in the ventral half of mesencephalic central gray matter. Before pharmacological testing, current intensity was reduced to yield stable, submaximal rates of self-stimulation. Rats were then injected daily with morphine for 10 days, and were tested three hours after injection. Between days 5 and 10 of treatment, many rats self-stimulated at more than 150% of baseline, but some others reduced self-stimulation to as little as 3% of baseline. Histological evaluation revealed that morphine facilitated self-stimulation when the electrode tip was located more than 0.3 mm from substantia nigra or more than 0.2 mm from the midline of central gray. In rats with electrode tips closer to substantia nigra or to the midline of central gray, morphine often reduced or failed to alter self-stimulation rates. The effects of a low dose of D-amphetamine (0.1 mg/kg) were investigated on electrode placements in the substantia nigra area. Placements close to the dorsal border of substantia nigra yielded less facilitation of self-stimulation by D-amphetamine than did placements located more dorsally or medially. Possible catecholaminergic substrates of these differential effects are discussed.

Animals↗
PubMed1977

Trigeminal substrates of intracranial self-stimulation in the brainstem.

Intracranial self-stimulation was elicited by electrodes located in the trigeminal motor nucleus of the rat. Rebound jaw movements were also elicited at postiive self-stimulation placements, but control experiments revealed that the lever pressing was not a motor artifact. It is suggested the modulation of trigeminal motoneurons may serve as an important reinforcement mechanism in the brainstem.

Animals↗
PubMed1992

Antidepressant treatment prevents chronic unpredictable mild stress-induced anhedonia as assessed by ventral tegmentum self-stimulation behavior in rats.

The effect of chronic unpredictable mild stress on sensitivity to reward was evaluated using the brain self-stimulation procedure. Rats were allowed to electrically self-stimulate the ventral tegmental area, one of the main cerebral structures subserving positive reinforcement. Stimulation thresholds (frequency of stimuli) for self-stimulation responses were determined prior to, during, and following a 19-day period of exposure to a variety of mild unpredictable stressors. Stimulation threshold was increased in stressed rats, suggesting a decrease in the rewarding properties of brain stimulation. This deficit became evident after about 1 week of mild stress, lasted throughout the stress period, and progressively diminished following termination of the stress regime. In stressed rats concomitantly treated with the tricyclic antidepressant desipramine (5 mg/kg b.i.d.), no stress-induced increase in self-stimulation threshold was observed. However, desipramine did not modify self-stimulation threshold in non-stressed animals. Thus, the increased threshold for brain self-stimulation produced by a period of chronic unpredictable mild stress can be completely prevented by concomitant antidepressant treatment and may provide an heuristic animal model of depression.

Animals↗
PubMed1977

Monoamine involvement in hippocampal self-stimulation.

The roles of noradrenergic and serotonergic projections to the hippocampus were investigated with respect to their involvement in the intracranial self-stimulation of this structure. In the first study, 6-hydroxydopamine-induced lesions of the dorsal tegmental noradrenergic bundle, which depleted hippocampal NE by 97%, had no effect on hippocampal self-stimulation in rats. In the second study, intragastric administration of para-chlorophenylalanine (PCPA) decreased hippocampal self-stimulation, suggesting the importance of a serotonin input in maintaining this behavior. Identical PCPA treatments resulted in temporary depletions of brain serotonin which paralleled the changes in hippocampal self-stimulation. The maximal decreases in both the biochemical and behavioral measures occured at 4 days post-drug. Interpretations of this deficit in hippocampal self-stimulation in terms of gross sensory and/or motor changes were ruled out as animals with lateral hypothalamic electrodes showed increases in self-stimulation paralleling the post-drug serotonin changes. An intra-sessional analysis of the PCPA-induced behavioral changes revealed that lateral hypothalamic self-stimulation was facilitated mainly during the first hour of the two-hour test sessions, whereas the depression in hippocampal self-stimulation occurred primarily in the last hour of the sessions. The differential effects of PCPA on lateral hypothalamic and hippocampal self-stimulation provide evidence against simple monoamine theories of reinforcement.

Animals↗